Glutamate and GABA Imbalance Following Traumatic Brain Injury

被引:351
作者
Guerriero, Rejean M. [1 ,2 ,3 ,4 ]
Giza, Christopher C. [5 ,6 ,7 ,8 ]
Rotenberg, Alexander [1 ,2 ,3 ,4 ]
机构
[1] Boston Childrens Hosp, Dept Neurol, Div Epilepsy, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA 02115 USA
[3] Boston Childrens Hosp, Dept Neurol, Brain Injury Ctr, Boston, MA 02115 USA
[4] Boston Childrens Hosp, Dept Neurol, Neuromodulat Program, Boston, MA 02115 USA
[5] Univ Calif Los Angeles, Div Pediat Neurol, Mattel Childrens Hosp, Brain Injury Res Ctr, Los Angeles, CA USA
[6] Univ Calif Los Angeles, Dept Neurosurg, Los Angeles, CA USA
[7] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA
[8] Univ Calif Los Angeles, Brain Injury Res Ctr, Dept Neurosurg, Semel Inst, Los Angeles, CA 90095 USA
关键词
Posttraumatic epilepsy; Parvalbumin interneuron; Glutamate transporter; NMDA receptor; TRANSCRANIAL MAGNETIC STIMULATION; RECEPTOR SUBUNIT EXPRESSION; RAT HIPPOCAMPUS; NMDA RECEPTORS; UP-REGULATION; POSTTRAUMATIC EPILEPSY; SYNAPTIC-TRANSMISSION; FLUID PERCUSSION; HEAD-INJURY; MEDIATED INHIBITION;
D O I
10.1007/s11910-015-0545-1
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Traumatic brain injury (TBI) leads to multiple short-and long-term changes in neuronal circuits that ultimately conclude with an imbalance of cortical excitation and inhibition. Changes in neurotransmitter concentrations, receptor populations, and specific cell survival are important contributing factors. Many of these changes occur gradually, which may explain the vulnerability of the brain to multiple mild impacts, alterations in neuroplasticity, and delays in the presentation of posttraumatic epilepsy. In this review, we provide an overview of normal glutamate and GABA homeostasis and describe acute, subacute, and chronic changes that follow injury. We conclude by highlighting opportunities for therapeutic interventions in this paradigm.
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页数:11
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